135 research outputs found

    Study on Unconventional Emergency Scenario Design: Taking Life-Rescuing of Dongfang Turbine Co., Ltd. in Wenchuan Earthquake for Example

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    Unconventional emergencies have attracted widespread concern in academic field due to its high uncertainty, huge destructiveness and complex management, and studies on unconventional emergencies shall change from “prediction-response” to “scenario-response”. By taking the life-rescuing of Dongfang Turbine Co., Ltd. in Wenchuan Earthquake for example, this paper divides scenarios in accordance with the specific investigations, and proposes several considerations about the unconventional emergency scenario study

    Tailoring the mechanical properties of 3D microstructures: a deep learning and genetic algorithm inverse optimization framework

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    Materials-by-design has been historically challenging due to complex process-microstructure-property relations. Conventional analytical or simulation-based approaches suffer from low accuracy or long computational time and poor transferability, further limiting their applications in solving the inverse material design problem. Here, we establish a deep learning and genetic algorithm framework that integrates forward prediction and inverse exploration. This framework provides an end-to-end solution to achieve application-specific mechanical properties by microstructure optimization. In this study, we select the widely used Ti-6Al-4V to demonstrate the effectiveness of this framework by tailoring its microstructure and achieving various yield strength and elastic modulus across a large design space, while minimizing the stress concentration factor. Compared with conventional methods, our framework is efficient, versatile, and readily transferrable to other materials and properties. Paired with additive manufacturing's potential in controlling local microstructural features, our method has far-reaching potential for accelerating the development of application-specific, high-performing materials.Comment: 19 pages, 5 figure

    Altered expression of Tim family molecules and an imbalanced ratio of Tim-3 to Tim-1 expression in patients with type 1 diabetes

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    BackgroundT-cell immunoglobulin and mucin domain (Tim) proteins are immunomodulatory molecules that play key roles in the regulation of T-cell activation. Published studies have reported that Tim molecules are involved in the pathogenesis of certain autoimmune diseases. Type 1 diabetes (T1D) is an autoimmune disease in which T cells mediate the destruction of islet β cells. However, the expression of Tim molecules in T1D remains unclear. In this study, we measured the expression of Tim family molecules as well as T-cell subset-specific transcription factors in T1D patients, and we explored the possible involvement of Tim molecules in the pathogenesis of T1D.MethodsNinety T1D patients, Thirty-six type 2 diabetes (T2D) patients and forty healthy controls (HCs) were recruited for this study. Peripheral blood mononuclear cells (PBMCs) were isolated, RNA was extracted from the PBMCs and reverse transcribed into cDNA, and gene expression patterns were analysed by RT–qPCR. The expression of Tim molecules in different T-cell subsets was analysed by flow cytometry.ResultsCompared with that in HCs, the mRNA expression of Tim-1 and RORC was increased in T1D patients (P=0.0355 and P=0.0423, respectively), while the expression of Tim-3 was decreased (P=0.0013). In addition, compared with HCs, the ratio of Tim-3 to Tim-1 expression in diabetic patients was decreased (P<0.0001 for T1D and P=0.0387 for T2D). The ratios of T-Bet to GATA3 expression and RORC to FOXP3 expression were higher in T1D patients than in HCs (P=0.0042 and P=0.0066, respectively). Furthermore, the T1D patients with defective islet function had more significant imbalances in the Tim-3/Tim-1 and RORC/FOXP3 ratios (P<0.0001, and P=0.001, respectively). Moreover, Both Tim-3 expression in CD4+ T cells and the Tim-3 to Tim-1 ratio were elevated in T1D in the remission phase compared to T1D.ConclusionOur study revealed altered expression of Tim molecules in T1D patients. The imbalanced ratios of Tim-3/Tim-1 expression were more pronounced in T1D patients with defective islet function. However, alterations in Tim molecule expression are mitigated in T1D in the remission phase. All these findings suggest that Tim family molecules may be involved in the pathogenesis of T1D

    Direct pro-inflammatory effects of prorenin on microglia

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    Neuroinflammation has been implicated in hypertension, and microglia have been proposed to play an important role in the progression of this disease. Here, we have studied whether microglia are activated within cardiovascular regulatory area(s) of the brain during hypertension, especially in high blood pressure that is associated with chronic activation of the renin-angiotensin-system. In addition, we determined whether prorenin, an essential component of the renin-angiotensin-system, exerts direct pro-inflammatory effects on these microglia. Our data indicate that two rodent models which display neurogenic hypertension and over activation of the renin-angiotensin-system in the brain (sRA mice and spontaneously hypertensive rats) exhibit microglial activation, and increased levels of pro-inflammatory cytokines, in the paraventricular nucleus of the hypothalamus, an area crucial for regulation of sympathetic outflow. Further, the renin-angiotensin-system component prorenin elicits directactivation of hypothalamic microglia in culture and induction of pro-inflammatory mechanisms in these cells, effects that involve prorenin receptor-induced NFκB activation. In addition, the prorenin-elicited increases in cytokine expression were fully abolished by microglial inhibitor minocycline, and were potentiated by pre-treatment of cells with angiotensin II. Taken together with our previous data which indicate that pro-inflammatory processes in the paraventricular nucleus are involved in the hypertensive action of renin-angiotensin-system, the novel discovery that prorenin exerts direct stimulatory effects on microglial activation and pro-inflammatory cytokine production provides support for the idea that renin-angiotensin-system -induced neurogenic hypertension is not restricted to actions of angiotensin II alone

    Thyroid function and associated mood changes after COVID-19 vaccines in patients with Hashimoto thyroiditis

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    ContextSevere acute respiratory syndrome-coronavirus 2 (COVID-19) vaccines may incur changes in thyroid functions followed by mood changes, and patients with Hashimoto thyroiditis (HT) were suggested to bear a higher risk.ObjectivesWe primarily aim to find whether COVID-19 vaccination could induce potential subsequent thyroid function and mood changes. The secondary aim was to find inflammatory biomarkers associated with risk.MethodsThe retrospective, multi-center study recruited patients with HT receiving COVID-19–inactivated vaccines. C-reactive proteins (CRPs), thyroid-stimulating hormones (TSHs), and mood changes were studied before and after vaccination during a follow-up of a 6-month period. Independent association was investigated between incidence of mood state, thyroid functions, and inflammatory markers. Propensity score–matched comparisons between the vaccine and control groups were carried out to investigate the difference.ResultsFinal analysis included 2,765 patients with HT in the vaccine group and 1,288 patients in the control group. In the matched analysis, TSH increase and mood change incidence were both significantly higher in the vaccine group (11.9% versus 6.1% for TSH increase and 12.7% versus 8.4% for mood change incidence). An increase in CRP was associated with mood change (p< 0.01 by the Kaplan–Meier method) and severity (r = 0.75) after vaccination. Baseline CRP, TSH, and antibodies of thyroid peroxidase (anti-TPO) were found to predict incidence of mood changes.ConclusionCOVID-19 vaccination seemed to induce increased levels and incidence of TSH surge followed by mood changes in patients with HT. Higher levels of pre-vaccine serum TSH, CRP, and anti-TPO values were associated with higher incidence in the early post-vaccine phase

    Genome sequence of the cultivated cotton <i>Gossypium arboreum</i>

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    The complex allotetraploid nature of the cotton genome (AADD; 2n = 52) makes genetic, genomic and functional analyses extremely challenging. Here we sequenced and assembled the Gossypium arboreum (AA; 2n = 26) genome, a putative contributor of the A subgenome. A total of 193.6 Gb of clean sequence covering the genome by 112.6-fold was obtained by paired-end sequencing. We further anchored and oriented 90.4% of the assembly on 13 pseudochromosomes and found that 68.5% of the genome is occupied by repetitive DNA sequences. We predicted 41,330 protein-coding genes in G. arboreum. Two whole-genome duplications were shared by G. arboreum and Gossypium raimondii before speciation. Insertions of long terminal repeats in the past 5 million years are responsible for the twofold difference in the sizes of these genomes. Comparative transcriptome studies showed the key role of the nucleotide binding site (NBS)-encoding gene family in resistance to Verticillium dahliae and the involvement of ethylene in the development of cotton fiber cells.Genetics &amp; HereditySCI(E)[email protected]; [email protected]; [email protected]

    GhWRKY6 Acts as a Negative Regulator in Both Transgenic Arabidopsis and Cotton During Drought and Salt Stress

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    Drought and high salinity are key limiting factors for cotton production. Therefore, research is increasingly focused on the underlying stress response mechanisms of cotton. We first identified and cloned a novel gene encoding the 525 amino acids in cotton, namely GhWRKY6. qRT-PCR analysis indicated that GhWRKY6 was induced by NaCl, PEG 6000 and ABA. Analyses of germination rate and root length indicated that overexpression of GhWRKY6 in Arabidopsis resulted in hypersensitivity to ABA, NaCl, and PEG 6000. In contrast, the loss-of-function mutant wrky6 was insensitive and had slightly longer roots than the wild-type did under these treatment conditions. Furthermore, GhWRKY6 overexpression in Arabidopsis modulated salt- and drought-sensitive phenotypes and stomatal aperture by regulating ABA signaling pathways, and reduced plant tolerance to abiotic stress through reactive oxygen species (ROS) enrichment, reduced proline content, and increased electrolytes and malondialdehyde (MDA). The expression levels of a series of ABA-, salt- and drought-related marker genes were altered in overexpression seedlings. Virus-induced gene silencing (VIGS) technology revealed that down-regulation of GhWRKY6 increased salt tolerance in cotton. These results demonstrate that GhWRKY6 is a negative regulator of plant responses to abiotic stress via the ABA signaling pathway
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